The functional properties of airway smooth muscle are fundamental to the
properties of the airways in vivo. However, many of the distinctive
characteristics of smooth muscle are not easily accounted for on the
basis of molecular models developed to account for the properties of
striated muscles. The specialized ultrastructural features and
regulatory mechanisms present in smooth muscle are likely to form the
basis for many of its characteristic properties.
The molecular organization and structure of the contractile apparatus in
smooth muscle is consistent with a model of force generation based on
the relative sliding of adjacent actin and myosin filaments, In airway
smooth muscle, actomyosin activation is initiated by the phosphorylation
of the 20 kDa light chain of myosin; but there is conflicting evidence
regarding the role of myosin light chain phosphorylation in tension
maintenance. Tension generated by the contractile filaments is
transmitted throughout the cell via a network of actin filaments
anchored at dense plaques at the cell membrane, where force is
transmitted to the extracellular matrix via transmembrane integrins.
Proteins bound to actin and/or localized to actin filament anchorage
sites may participate in regulating the shape of the smooth muscle cell
and the organization of its contractile filament system. These proteins
may also participate in signalling pathways that regulate the
crossbridge activation and other functions of the actin cytoskeleton.
The length-dependence of active force and the mechanical plasticity of
airway smooth muscle may play an important role in determining airway
responsiveness during lung volume changes in vivo. The molecular basis
for the length-dependence of tension in smooth muscle differs from that
in skeletal muscle, and may involve mechano-transduction mechanisms that
modulate contractile filament activation and cytoskeletal organization
in response to changes in muscle length. The reorganization of
contractile filaments may also underlie the plasticity of the mechanical
response of airway smooth muscle, Changes in the structural organization
and signalling pathways of airway smooth muscle cells resulting form
alterations in mechanical forces in the lung may be important factors in
the development of pathophysiological conditions of chronic airway
hyperresponsiveness.
%0 Journal Article
%1 gun-tan
%A Gunst, SJ
%A Tang, DD
%C 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK
%D 2000
%I MUNKSGAARD INT PUBL LTD
%J EUROPEAN RESPIRATORY JOURNAL
%K asm contractile
%N 3
%P 600-616
%R 10.1034/j.1399-3003.2000.15.29.x
%T The contractile apparatus and mechanical properties of airway smooth
muscle
%V 15
%X The functional properties of airway smooth muscle are fundamental to the
properties of the airways in vivo. However, many of the distinctive
characteristics of smooth muscle are not easily accounted for on the
basis of molecular models developed to account for the properties of
striated muscles. The specialized ultrastructural features and
regulatory mechanisms present in smooth muscle are likely to form the
basis for many of its characteristic properties.
The molecular organization and structure of the contractile apparatus in
smooth muscle is consistent with a model of force generation based on
the relative sliding of adjacent actin and myosin filaments, In airway
smooth muscle, actomyosin activation is initiated by the phosphorylation
of the 20 kDa light chain of myosin; but there is conflicting evidence
regarding the role of myosin light chain phosphorylation in tension
maintenance. Tension generated by the contractile filaments is
transmitted throughout the cell via a network of actin filaments
anchored at dense plaques at the cell membrane, where force is
transmitted to the extracellular matrix via transmembrane integrins.
Proteins bound to actin and/or localized to actin filament anchorage
sites may participate in regulating the shape of the smooth muscle cell
and the organization of its contractile filament system. These proteins
may also participate in signalling pathways that regulate the
crossbridge activation and other functions of the actin cytoskeleton.
The length-dependence of active force and the mechanical plasticity of
airway smooth muscle may play an important role in determining airway
responsiveness during lung volume changes in vivo. The molecular basis
for the length-dependence of tension in smooth muscle differs from that
in skeletal muscle, and may involve mechano-transduction mechanisms that
modulate contractile filament activation and cytoskeletal organization
in response to changes in muscle length. The reorganization of
contractile filaments may also underlie the plasticity of the mechanical
response of airway smooth muscle, Changes in the structural organization
and signalling pathways of airway smooth muscle cells resulting form
alterations in mechanical forces in the lung may be important factors in
the development of pathophysiological conditions of chronic airway
hyperresponsiveness.
@article{gun-tan,
abstract = {{The functional properties of airway smooth muscle are fundamental to the
properties of the airways in vivo. However, many of the distinctive
characteristics of smooth muscle are not easily accounted for on the
basis of molecular models developed to account for the properties of
striated muscles. The specialized ultrastructural features and
regulatory mechanisms present in smooth muscle are likely to form the
basis for many of its characteristic properties.
The molecular organization and structure of the contractile apparatus in
smooth muscle is consistent with a model of force generation based on
the relative sliding of adjacent actin and myosin filaments, In airway
smooth muscle, actomyosin activation is initiated by the phosphorylation
of the 20 kDa light chain of myosin; but there is conflicting evidence
regarding the role of myosin light chain phosphorylation in tension
maintenance. Tension generated by the contractile filaments is
transmitted throughout the cell via a network of actin filaments
anchored at dense plaques at the cell membrane, where force is
transmitted to the extracellular matrix via transmembrane integrins.
Proteins bound to actin and/or localized to actin filament anchorage
sites may participate in regulating the shape of the smooth muscle cell
and the organization of its contractile filament system. These proteins
may also participate in signalling pathways that regulate the
crossbridge activation and other functions of the actin cytoskeleton.
The length-dependence of active force and the mechanical plasticity of
airway smooth muscle may play an important role in determining airway
responsiveness during lung volume changes in vivo. The molecular basis
for the length-dependence of tension in smooth muscle differs from that
in skeletal muscle, and may involve mechano-transduction mechanisms that
modulate contractile filament activation and cytoskeletal organization
in response to changes in muscle length. The reorganization of
contractile filaments may also underlie the plasticity of the mechanical
response of airway smooth muscle, Changes in the structural organization
and signalling pathways of airway smooth muscle cells resulting form
alterations in mechanical forces in the lung may be important factors in
the development of pathophysiological conditions of chronic airway
hyperresponsiveness.}},
added-at = {2013-01-07T13:13:03.000+0100},
address = {{35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK}},
affiliation = {{Gunst, SJ (Reprint Author), Indiana Univ, Sch Med, Dept Physiol \& Biophys, 635 Barnhill Dr, Indianapolis, IN 46202 USA..
Indiana Univ, Sch Med, Dept Physiol \& Biophys, Indianapolis, IN 46202 USA.}},
author = {Gunst, SJ and Tang, DD},
biburl = {https://www.bibsonomy.org/bibtex/2bc2dcf515bdf8ed94b35bfb13f997836/jehiorns},
doc-delivery-number = {{295JG}},
doi = {{10.1034/j.1399-3003.2000.15.29.x}},
interhash = {d00527b111612fde6745af2eb08e0ce7},
intrahash = {bc2dcf515bdf8ed94b35bfb13f997836},
issn = {{0903-1936}},
journal = {{EUROPEAN RESPIRATORY JOURNAL}},
journal-iso = {{Eur. Resp. J.}},
keywords = {asm contractile},
keywords-plus = {{LIGHT-CHAIN KINASE; CROSS-BRIDGE PHOSPHORYLATION; ACTIN-BINDING PROTEIN;
ISOTONIC SHORTENING VELOCITY; VERTEBRATE NON-MUSCLE; MYOSIN
PHOSPHORYLATION; THIN-FILAMENTS; ALPHA-ACTININ; CHICKEN GIZZARD; CA2+
SENSITIVITY}},
language = {{English}},
month = {{MAR}},
number = {{3}},
number-of-cited-references = {{201}},
pages = {{600-616}},
publisher = {{MUNKSGAARD INT PUBL LTD}},
research-areas = {{Respiratory System}},
times-cited = {{76}},
timestamp = {2013-01-07T13:13:03.000+0100},
title = {{The contractile apparatus and mechanical properties of airway smooth
muscle}},
type = {{Review}},
unique-id = {{ISI:000085962500029}},
volume = {{15}},
web-of-science-categories = {{Respiratory System}},
year = {{2000}}
}